Studies on patients hospitalized for a variety of sytemic diseases (sepsis, liver disease, pulmonary disease, malignancy) show that many of these patients have elevated circulating serum inhibitors of mouse bone marrow colony formation. The inhibition of colony formation by patient serum is significantly higher in anergic patients and patients with demonstrable serum chemotactic inhibitory activity. Studies show that peripheral blood polymorphonuclear leukocyte counts are not reduced when bone marrow colony formation inhibitors are present although peripheral blood monocyte counts are significantly less than those in patients without inhibitory acitivity. Suppression appears to be cell directed and due to multiple serum factors, both heat labile and heat stable. Partial characterization of one factor indicates a molecular weight of greater than 200,000, a density of greater than 1.006 and no association with alpha or beta lipoprotein. Additional experiments dealing with serum from myeloma patients indicate that neutrophil chemotactic inhibitors are prevalent in serum from patients with IgA myeloma and not in sera from patients with IgG myeloma or Waldenstrom's macroglobulinemia. Inhibitory activity is associated with the IgA M-component, cell directed, dependent upon an intact Fc portion of the IgA and associated primarily with polymeric forms of the immunoglobulin. Studies show that IgA mediated inhibition of leukocyte chemotaxis affects both neutrophils and eosinophils with a much lesser effect on monocytes. The mechanism of this inhibition and relationship to the suppression of leukocyte function is currently under investigation.